

Poster 174:
Subacute Combined Degeneration of the Spinal Cord
(Lichtheim’s Disease)
Quoc P. Tran, MD (Carolinas Med Cntr, Charlotte, NC, United States))
Disclosures:
Quoc Tran: I Have No Relevant Financial Relationships To
Disclose
Case/Program Description:
A 54-year-old man with a history of ane-
mia, alcoholism, and diabetes presented with increasing weakness,
tremors, gait instability, altered mental status and dysesthesias. CT
head and MRI brain were negative. His diabetes was well controlled
and he denied any history of neuropathy.
Setting:
Tertiary Care Hospital.
Results:
MRI of the cervical spine revealed increased signal from C2 to
T1 predominantly in the dorsal aspect of the cord. Laboratory data
revealed megaloblastic anemia, vitamin B12 level was markedly
reduced (
<
50 pg/mL) and methylmalonic acid level was significantly
elevated (23990). Intrinsic factor antibodies were also positive (67.4).
Homocysteine level was also elevated at 273
m
mol/L. The patient was
diagnosed with subacute degeneration of the spinal cord secondary to
pernicious anemia. Cobalamin replacement was initiated with gradual
recovery of his motor function, sensory deficits and cognition.
Discussion:
Subacute combined degeneration of the spinal cord is a
rare demyelinating disorder that primarily affects the dorsal and
lateral columns of the spinal cord. It is typically secondary to cobal-
amin deficiency but can be due to vitamin E and copper deficiency. Our
patient had a history of pernicious anemia, which gradually led to his
decline in motor and sensory function. Homocysteine levels may be
the only elevated marker with normal cobalamin levels in certain
patients. Patients can regain significant recovery within the first
month of cobalamin replacement therapy. Delayed treatment can
result in permanent deficits in sensation and motor function.
Conclusions:
Subacute combined degeneration of the spinal cord is a
condition that can affect both motor (corticospinal) and sensory (dorsal
column) tracts and is easily treatable if identified early. Permanent
changes can be observed with delayed diagnosis and treatment. Phy-
sicians need to be aware of this rare disorder while evaluating a patient
with weakness and dysesthesia in the setting of vitamin B12 deficiency.
Level of Evidence:
Level V
Poster 175:
Heterotopic Ossification of the Hip in Intensive Care
Unit-Acquired Weakness: A Case Report
Xiaoning Yuan, MD, PhD (NY Presby Hosp/Columbia/Cornell, New York,
New York, United States), Rosa S. Cho, MD, Diane A. Thompson, MD
Disclosures:
Xiaoning Yuan: I Have No Relevant Financial Relation-
ships To Disclose
Case/Program Description:
A 52-year-old man with history of
emphysema was admitted for bilateral lung volume reduction surgery.
His post-operative course was complicated by acute respiratory failure
and acute kidney injury (AKI). He was hospitalized for 4.5 months,
including 3 months in the intensive care unit (ICU). At the time of
rehabilitation consultation, he reported bilateral lower extremity
(BLE) neuropathic pain. Physical exam was notable for decreased BLE
reflexes and strength: bilateral shoulder abduction 4/5, elbow flexion
5/5, wrist extension 5/5, hip flexion 3/5, knee extension 4/5, ankle
dorsiflexion 1/5. ICU-acquired weakness (ICUAW) was diagnosed based
on a Medical Research Council (MRC) score of 44. He began rehabili-
tation, but had persistent left hip pain and tightness with therapy.
Initially, the tightness was thought to be spasticity. His symptoms
improved slightly with baclofen and increasing gabapentin for neuro-
pathic pain, but persisted 2 weeks into his rehabilitation course.
Setting:
Inpatient rehabilitation unit.
Results:
A left hip radiograph was obtained and demonstrated a large
amount of heterotopic ossification (HO) but no fracture or dislocation.
Review of his labs revealed markedly elevated alkaline phosphatase
(ALP) starting 1 month into his ICU stay, but normalizing by the end of
his rehabilitation course.
Discussion:
While HO is a known complication in polytrauma and burn
patients, it should be considered earlier in ICUAW patients. Radiography is
typically sufficient for diagnosis. Treatment is indicated if risk factors and
signs of progressive HO persist. We opted against medical management for
this patient as his mobility was improving and ALP no longer elevated. We
continued passive range of motion during therapy, discontinued baclofen,
and deferred non-steroidal anti-inflammatory drugs due to resolving AKI.
Conclusions:
HO should be investigated in ICUAW patients with
persistent pain and stiffness that does not resolve with conservative
therapies. Early ICU rehabilitation may prevent HO development.
Level of Evidence:
Level V
Poster 176:
Enoxaparin Induced Tissue Necrosis: A Case Report
Molly E. Schill, DO (Vidant Rehab Ctr/East Carolina Univ/Brod),
Clinton E. Faulk, MD, FAAPMR
Disclosures:
Molly Schill: I Have No Relevant Financial Relationships
To Disclose
Case/Program Description:
A morbidly obese 67-year-old female
trauma patient with no known allergies presented to inpatient rehabili-
tation following open reduction internal fixation of a tibial plateau fracture
andwas started on enoxaparin for deep vein thrombosis (DVT) prophylaxis.
She developed a large, black ecchymotic area on her left lower abdomen
10 days after initial dose. Ultrasound was negative for fluid collection.
Patient remained afebrile without leukocytosis and did not develop
thrombocytopenia. The area progressed to necrosis the following day.
Dermatology was consulted and recommended continuing enoxaparin as
the area likely resulted from damage to a vessel from injection technique.
Therapies were initially held due to pain at the site and further work up.
Setting:
Academic Inpatient Rehabilitation Center.
Results:
5 days after continuation of enoxaparin, she developed a
second large ecchymotic area on her right lower quadrant abdomen at
a subsequent injection site. Enoxaparin was then stopped and oral
rivaroxaban was started for DVT prophylaxis. By discharge, the ne-
crosis over the first wound fell off revealing red granulation tissue and
the second ecchymotic area resolved without necrosis. She had follow
up made with the wound care clinic.
Discussion:
Enoxaparin is very commonly used for prevention of DVT in
inpatient rehabilitation. There are few case reports of enoxaparin-
induced tissue necrosis and the pathogenesis remains poorly understood.
Most cases occur 4-12 days following initial injection. Proposed mecha-
nisms includeHITsyndrome, hypersensitivity reactions, local trauma, and
high concentrations of drug from reduced absorption fromadipose tissue.
Therapies can be disrupted due to pain or further work-up.
Conclusions:
Enoxaparin-induced tissue necrosis is a rare adverse
effect. Because many patients are admitted to rehabilitation in the
time frame in which necrosis starts appearing, physicians should be
vigilant in examining injection areas and discontinue treatment early
if necrosis develops to prevent further complications.
Level of Evidence:
Level V
Poster 177:
End-Stage Heart Failure Requiring Intra-Aortic
Balloon Pump Complicated by a Cerebrovascular
Accident and Femoral Neuropathy Are Rehabilitation
Challenge
Yonghoon Lee, MD (Albert Einstein Col of Med), Eathar Saad, MD
Disclosures:
Yonghoon Lee: I Have No Relevant Financial Relationships
To Disclose
Case/Program Description:
A 50-year-old man with end-stage heart
failure with ejection fraction of 10-15 % secondary to extensive
S188
Abstracts / PM R 9 (2017) S131-S290